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CardioRhythm
by Jim English
Sudden cardiac death, resulting from untreated
rapid ventricular fibrillation, is the leading cause of death in
the United States, affecting about 400,000 people each year and
claiming the lives of about 70% of them. Sudden cardiac death occurs
most often in people who have had heart attacks (myocardial infarction)
in the past, but can also occur in young people who were entirely
well until the time of death. Ischemia, caused by a lack of oxygen
to the heart due to narrowing of the coronary arteries, can lead
to cardiac arrest, a heart attack from a sustained ventricular arrhythmia.
A number of natural agents have been shown to
prevent the occurrence of arrhythmias while supporting normal heart
rhythm and improving cardiac function. Some of these benefits include
a positive inotropic effect (increased strength of heart contractions),
increased myocardium (heart) tissue oxygenation, and scavenging
of free radicals. Working by different complementary mechanisms,
these natural compounds produce anti-arrhythmic actions and benefit
cardiac functions without the side effects associated with some
antiarrhythmic drugs.
Berberine, the active ingredient found in the herb goldenseal (Hydrastis
canadensis) has been shown to be beneficial for ventricular
arrhythmias caused by lack of oxygen. Evidence also suggests that
berberine administration can help prevent the onset of re-entrant
ventricular tachyarrhythmias and sudden coronary death after myocardial
ischemic damage.
The effects of berberine on individuals with ventricular
tachyarrhythmias showed that 62% of patients had 50% or greater,
and 38% of patients had 90% or greater, suppression of ventricular
premature contractions. No severe side effects were observed from
berberine therapy. In humans with refractory congestive heart failure,
berberine produced several significant changes: a 48% decrease in
systemic and a 41% decrease in pulmonary vascular resistance, along
with a 28% decrease in right atrium and 32% decrease in left ventricular
end-diastolic pressures. A measurable increase in cardiac index
(45%), stroke index (45%), and left ventricular ejection fraction
(56%) was also observed.
Myocardial biopsies of patients with various cardiac diseases showed
a CoQl0 deficiency in up to 75% of cases!9 Research has shown that
orally administered CoQl0 can improve functioning of myocardial
tissue, strengthening the heart’s contractions and making
it beat more strongly and more regularly. CoQ10 also acts as an
antioxidant to control free radicals produced during cardiac interventions
(including angioplasty, thrombolysis, and surgery).
Accordingly, CoQl0 has been used in the treatment
of different heart disorders that include arrhythmias related to
primary cardiomyopathies or secondary forms of heart failure. A
1998 study observed patients with acute myocardial infarction. For
28 days one group received 120 mg of CoQ10 and the other group received
a placebo. After treatment, total arrhythmias were only 9.5% in
the CoQ10 group compared to 25.3% in the placebo group. CoQ10 produced
a significant reduction in angina pectoris and left ventricular
dysfunction. Non-fatal infarction and cardiac deaths also were significantly
lower in the CoQ10 group.
Taurine modulates the activity of cAMP and affects enzymes in heart
muscle that contribute to contractility. Taurine also plays a role
in the metabolism of calcium and may affect entry of calcium into
heart muscle cells where it is essential in the generation and transmission
of nerve impulses. Research shows that taurine prevents arrhythmogenesis
by limiting cardiac hypertrophy and calcium overload of the myocardium.
Taurine also protects the heart against reperfusion-induced arrhythmias
via its properties as a membrane stabilizer and as an oxygen free
radical scavenger.
Arrhythmias characteristic of acute myocardial
ischemia may be due to loss of intracellular taurine. Researchers
found that intravenous administration of taurine prevented arrhythmias
caused by digitalis. Taurine also inhibited the drop in potassium
levels inside heart cells, which can cause electrical instability
and arrhythmias. Supplemental taurine has been shown to reduce the
occurrence of myocardial infarction and to lower elevated blood
pressure by reducing sympathetic tone.
References
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Fact sheet, National Heart, Lung and Blood Institute, NIH Publication
No. 95-2264, September 1995.
2. Managing Ventricular Fibrillation in Patients with Silent Myocardial
Ischemia Reprinted from Medical Sciences Bulletin 9/13/99, published
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3. D. Sheffield, et al. Results from the Psychophysiological Investigation
of Myocardial Ischemia (PIMI) Study. Ref: 48th annual meeting of
the American College of Cardiology. March, 1999.
4. Podrid PJ, Lampert S, Graboys TB, Blatt CM, Lown B. Aggravation
of arrhythmia by antiarrhythmic drugs - incidence and predictors.
Am J Cardiol 1987;59:38E-44E.
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1988;11:253-260.
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Sci., U.S.A., vol. 82(3), pp 901-904.
10. Mortensen S.A., Vadhanavikit S., Muratsu K., Folkers K. (1990)
Int. J. Tissue React., Vol. 12 (3), pp 155-162.
11. Singh RB; Wander GS et al Cardiovasc Drugs Ther, 12(4):347-53
1998 Sep.
12. Sebring, L. A. and Huxtable, R. J. Sulfur Amino Acids: Biochemical
& Clinical Aspects, 1983.
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S. Res. Commun. Chem. Patho. Pharma., 43(2):343-346, 1984.
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J. Pharmacol, 98:269-273, 1984.
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